Physiological mechanisms of increased activity-related dyspnea in obesity

Obesity is an independent risk factor for troublesome activity-related dyspnea. The mechanisms of increased exertional dyspnea in obesity remain poorly understood and represented the primary focus of our study. To this end, ventilation (V_E), breathing pattern, dynamic operating lung volume, diaphragm EMG activity expressed as a percentage of maximum (EMGdi%max; an index measure of neural respiratory drive) and dyspnea responses to symptom-limited incremental cycle exercise testing were compared between 30 obese (OB; 15M:15W; mean±SE BMI=33.6±0.8 kg/m²; 43±1% fat mass; 137±3% ideal body mass) and 30 non-obese (NOB; 15M:15W; BMI=21.8±0.3 kg/m²; 28±1% fat mass; 89±1% ideal body mass) adults aged 18-40 yrs. After adjusting for differences in lean body mass (OB, 56±2 vs. NOB, 46±2 kg), V_E, breathing frequency, EMGdi%max and dyspnea were higher at any standardized submaximal work rate during exercise in OB vs. NOB. Mean values of inspiratory capacity (IC) and inspiratory reserve volume (IRV) were higher (by ∼260 mL and ∼400 mL, respectively) at rest and at any V_E during exercise in OB vs. NOB. Interestingly, EMGdi%max-IRV and dyspnea-IRV relationships were parallel shifted to the left during exercise in OB vs. NOB. By contrast, EMGdi%max-V_E, dyspnea-V_Eand dyspnea-EMGdi%max relationships were similar throughout much of exercise in OB vs. NOB. In conclusion, mechanical adaptations of the respiratory system, including recruitment of resting (pre-exercise) IC and IRV, helped to preserve EMGdi%max-V_E relationships during exercise in OB vs. NOB. Under these circumstances, the increased perception of exertional dyspnea in OB likely reflected the awareness of increased neural respiratory drive.